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The loss of smell is one of the most frequent symptoms during a SARS-CoV-2 infection. This type of symptom, even though it is more rare for respiratory viruses like the flu, is however, well known and associated with the virus' ability to infect olfactory nerves. However, these neurves are exposed to the environment and are directly connected to the central nervous system (CNS). A virus capable of infecting could also access the CNS through the olfactory nerves. A high number of patients have had neurological manifestations, notably for the more severe cases of Covid-19, suggesting that SARS-CoV-2 could invade the SNC. Within this context, it is important to understand the interactions between the olfactory neurons and this virus.

SARS CoV-2 enters cells using a specific receptor called ACE2. The olfactory neurons present in the nose are surrounded by support cells called sustentacular cells that have this ACE2 specific receptor, whereas neurons do not express it. Their studies showed that in the hamster, SARS-CoV-2 massively infests sustentacular cells but not olfactory nerves. They observed that in addition to infection of support cells, there is also a desquamation of the nasal mucosa, which could explain the loss of smell. Indeed, desquamation of the nasal musoca leads to a loss of olfactory nerves responsible for odor detection. Even if the mechanism in man is the same as that observed in infected hamsters, it could be responsible for the origin of the anosmia observed and would prevent the virus from penetrating into the SNC via the olfactory system as has recently been suggested.²

Luckily, the nasal mucosa is capable of regenerating itself throughout life due to pluripotent cells³. In their experiments, researchers observed a 50% recuperation of the initial nasal mucosa at 14 days after the start of the infection.